RVF is an acute viral disease of sheep, cattle, goats and humans.
It is manifested with hepatitis and high mortality in young lambs
and calves, and abortion in adult animals. Rift valley fever
resembles influenza in humans. The disease is of significant
importance in Africa.

Transmission : Biting insects and mosquitoes. Possible direct
contact via cornea. Human infection occur by handling diseased
tissues, and strict precautions should be instituted to prevent
infection with this virus, such as wearing goggles and gloves.

Antemortem findings :

Sheep

Incubation 12 – 48 hours in young animals

High morbidity and mortality in lambs and calves

Fever

Lambs refuse to eat, have abdominal pain and are
recumbent.

Animals seek a shaded area because of photophobia
(squinting and blinking)

Photosensitization characterized with a thickened head and
ears.

Encrustation around the muzzle (Fig. 149)

Vomiting in adult animals

Congenital malformation of the brain and muscles

Abortion in ewes during the illness or convalescence

Cattle

Edematous unpigmented skin showing cracking and
sloughing due to photosensitization

Salivation and inflammation in the mouth

Abdominal pain

Diarrhoea associated with haemorrhagic inflammation of
stomachs and intestine

Lameness

Cessation of milk production

Abortion

Postmortem findings :

Cyanotic visible mucosae

Necrosis of the liver in lambs (liver may be mottled grey, or
reddish-brown to bright yellow in colour)

Judgement : Carcass of an animal showing clinical signs of Rift
Valley fever is condemned. Reactors and recovered animals are
approved. Affected parts of the carcass, liver and the blood must
be condemned.

A highly infectious pox virus disease of sheep and goats
manifested by the occurrence of the pustular and scabby lesions on
the lips, muzzle and udder.

Transmission : Direct contact between animals. Indirect contact
with dry scabs in pens. The virus is resistant to drying and may be
viable in scabs for months and years in empty feedlots and pens.
Farm workers may disseminate the virus among animals of
different pens with contaminated equipment, feed and farm
vehicles.

Antemortem findings :

Incubation: 2 – 3 days

Pustular and scabby lesions on the muzzle (Fig. 151), lips
and eyes.

Lesions on the udder and teats and the coronary band

The invasion of lesions by larvae of the screw worm fly and
secondary bacterial ection with Fusobacterium necrophorum

Lambs and kids are unable to suckle or graze due to lip
lesions.

Uncomplicated cases may heal within one month.

Emaciation

Pneumonia in feeder lambs

Postmortem findings :

Pustular and scabby lesions on the head, udder and feet

Ulcerative lesions in the nasal cavity and erosions in the
mucosa of the oesophagus and upper respiratory tract.

Inflammation of the reticulum, omasum and intestine

Necrotic lesions in the lungs, pleura and liver

Judgement : The carcass is condemned if the disease is
accompanied with inflammation of the stomachs and intestines, and
with bronchopneumonia. Otherwise, it is approved.

Bluetongue is a highly contagious viral disease of sheep,
manifested by fever, oral lesions, lameness and emaciation. The
disease occurs mostly in the African region, but also in Asia and
the Pacific and in the Western hemisphere, but can be well
controlled by vaccination.

Sheep and goat pox is a contagious viral disease of sheep and
goats manifested by papular and pustular eruptions on the skin and
in generalized conditions with haemorrhagic inflammation of the
respiratory tract.

Skin lesions may vary from macules, papules, vesicles,
pustules to pocks and scabs.

Necrosis and coalescing of the lesions and loss of wool (Fig.
156)

Clinical signs of goat pox are less severe than in sheep pox.
The benign form of sheep pox is commonly found in adult
sheep and the malignant form in lambs.

Postmortem findings :

Reddish to whitish firm nodules in the mucosa of the
pharynx and trachea

Reddish to whitish nodules in the lungs (Fig. 157). Rarely
pneumonia

In malignant form: inflammation of the respiratory and
digestive tract

Judgement : Carcass of an animal showing the clinical disease
without secondary complications is conditionally approved pending
heat treatment. The recovered animals are approved. The carcass
is condemned if the acute febrile or pustular stage of the disease
is associated with secondary bacterial infections or if the carcass
is inadequately bled. If bacteriological examination showed
negative results, this carcass may be conditionally approved
pending heat treatment.

Scrapie is a chronic disease of the central nervous system in
sheep and occasionally goats characterized by itching, nervous
signs and a long incubation period. It is caused by a viral agent
called “viroid” or “prion”, which has some of the characteristics
of the virus, a “slow” virus like BSE and Maedi.

Transmission : Most likely, the organism enters through breaks
in the skin and mucous membranes of susceptible sheep. The agent
is present in the lymph nodes, spleen, spinal cord and brain of
infected sheep. It is transmitted from sick animals to healthy
animals through pasture, where it may be infective for over 3
years. Vertical transmission from the dam and possibly the sire in
sheep may also occur. The disease may be transmitted by
inoculation of infective material. The agent is resistant to rapid
freezing, thawing, boiling for 30 minutes and even to a 20 %
formalin solution. At temperatures of 0 – 4°C, the prion is still
active after two years. Oscillation of the temperature from 37–
70°C does not affect its infectivity. At temperatures of 94–98°C,
the prion is still resistant for 24 hours.

Antemortem findings :

Dry wool and rough skin

Loss of wool from the head down over the side of the face,
rump, thigh, tail base and abdomen

Changes of behaviour. Charging of fences, dogs etc.

Biting of legs, flanks and belly because of severe itchiness
(pruritus)

Smacking and rarely curling of the lips and wagging of the
tail during rubbing of the skin over the back and sacrum

Grinding the teeth

Twitching of muscles, excitability and wild expression of the
eyes

Restless animal, continuously laying down and getting up

Incoordinated gait, tendency to run and fall down.

Convulsions

Postmortem findings :

No gross lesions observed

Microscopy reveals the presence of large vacuoles in the
cytoplasm of neurons; this is considered a diagnostic lesion.

Judgement : Carcass and viscera affected with the clinical disease
are condemned. Carcass of contact animals, offspring and
ancestors may have a limited distribution or it may be condemned
if economically feasible.

Pulmonary adenomatosis is a chronic progressive pneumonia of
sheep with the development of a primary lung neoplasm. This
neoplasm is carcinomatous and infrequently metastatic to regional
lymph nodes. A retrovirus causes the disease and a herpesvirus
acts in a secondary role. This is a disease of old ewes, more then
4 years of age. Lambs and yearling are rarely affected.

Transmission : The disease is experimentally transmitted by
inhalation of infected droplets by sheep that are kept in close
contact. Vertical transmission from pregnant ewes to fetus has also
been demonstrated.

Antemortem findings :

Incubation 2 months to 2 years

Difficult breathing and lacrimation

Loss of weight and emaciation

When the rear of a sheep is lifted, excess fluid will run from
the nose (wheel barrow test).

Emaciation and lacrimation

Postmortem findings :

The lungs are increased in size and weight (as much as triple
their normal size) and do not collapse when the thoracic
cavity is opened (Fig. 159).

Bluish grey consolidation of the ventral part of the lung

Secondary bacterial infections in the lungs

Focal lung lesions are interspersed with areas of emphysema.

Metastasis of the neoplasm into the bronchial and mediastinal
lymph nodes may occur infrequently.

Judgement : Carcass judgement depends on the extent of lung
involvement, condition of the carcass and secondary bacterial
infection. Extensive lung lesions with metastasis and loss of
musculature would necessitate the condemnation of the carcass.

Nairobi sheep disease is a non contagious, tick borne viral
disease in sheep manifested by acute haemorrhagic inflammation
of the stomach and intestine and by respiratory signs.

Transmission : Adult forms of a tick Rhipicephalus appendiculatus
which attach themselves inside the ear of an animal. Unfed adult
ticks are infective for one year. Faeces does not contain the virus.

Antemortem findings :

Incubation 4 – 15 days

Fever; during fever the blood, urine and tissue are infective

Rapid painful breathing

Dullness and depression

Mucopurulent nasal discharge

Pain and grunting with defecation

Acute haemorrhagic gastroenteritis

Bright to dark green faeces (is important in the differential
diagnosis.)

Abortion in pregnant ewes

Swollen vulva and external genitalia

Collapse and death

Postmortem findings :

Excess fluid in the pericardium

Ecchymotic and petechial haemorrhage in the heart muscle

Acute haemorrhagic inflammation of the stomachs (Fig. 161)
and intestine

Distended gall bladder contains thick syrupy bile

Enlarged and edematous lymph nodes

Hyperaemic genital tract

Judgement : Carcass of an animal affected with the acute disease
accompanied with fever and acute gastrointestinal lesions is
condemned. Carcass of recovered animals and of animals with non
systemic or generalized lesions is approved. The affected organs
are condemned.

Differential diagnosis : Rift Valley fever in sheep. Diarrhoea in
RVF may show blood tinged watery faeces, but is not green in
colour as in NSD. In rinderpest ulcerative lesions are noted with
bloody (and not green) faeces. Heartwater, anthrax and plant
poisoning should also be considered in differential diagnosis.

Transmission : By inhalation; carrier or infected animals may also
bring the infection into the flock.

Antemortem findings :

Incubation: 6 – 10 days

Extremely infective with morbidity of 100 %

Acute disease with mortality of 60 – 70 %

Fever

Cough

Tongue sticking out and frothy salivation

Mouth breathing in terminal stage

Lagging and frequently laying

Death in few days

Postmortem findings :

Fibrinous inflammation of the pleura (Fig. 162)

Slight interlobular pulmonary reaction. Lesion may be
present in only one lung.

Pleural adhesions

Enlarged mediastinal lymph nodes

No sequestration of necrotic areas as in cattle

Judgement : Carcass of an animal affected with contagious
caprine pleuropneumonia which shows no systemic involvement is
approved. The affected organs are condemned. The septicemic
form of the disease calls for carcass condemnation.

Black quarter is an acute infectious disease of sheep and cattle
manifested by inflammation of the muscles, toxaemia and high
mortality. It is caused by Clostridium chauvoei.

Transmission : Contaminated soil. The organisms enter into the
digestive tract with feed and through cuts which occur during the
shearing, docking, and castration, and via naval infection during
birth. Infection of the vulva and vagina of the ewes during lambing
may cause serious outbreak of the disease. Black leg is worldwide
in distribution. Well nourished and grass fed animals are more
often affected.

Antemortem findings :

Fever

Loss of appetite

Depression

Stiff gait and reluctance to move due to lameness

Subcutaneous edema is not common.

Gaseous crepitation occurs before death.

Head lesions associated with edema and nose bleeding

Postmortem findings :

Subcutaneous edema particularly noted around head.

Affected muscle is dark brown, dry and sponge like or
moist. A pungent odour is noted. Less gas is formed than in
cattle.

Genital tract lesions in the walls of the vagina and
occasionally uterus

Serosanguineous and haemorrhagic fluid in body cavities and
pericardial sac

Edema of lungs

Judgement : Total condemnation of the carcass and viscera of an
animal affected with black leg. It is prohibited to slaughter and
dress the animal diagnosed with this disease on antemortem
examination.

This disease is a fatal toxaemia in lambs, sheep, goats, calves
and seldom in adult cattle. The disease is manifested by diarrhoea,
involuntary contraction of muscles, paralysis and sudden death. It
occurs after a sudden change to a better, more nutritious diet. The
disease is often noted in sheep that have been fed heavy grain, and
in animals which graze on lush growing pastures. Clostridium
perfringens multiplies in abomasum and intestine and produces
toxin which paralyses the vital centres in brain and damages
endothelium of blood vessels. The disease occurs extensively in
particular in Southern Africa but is well controlled by vaccination.

Antemortem findings :

Short course of the illness (2 – 12 hours) in lambs and longer
course (24 hours) in sheep

Animal found dead without previous sign of the disease

Dullness and depression

Rapid shallow respiration

Loss of appetite and frothing

Muscular contractions

Green pasty diarrhoea

Grinding of the teeth and muscular tremor

Logging behind the flock

Staggering and recumbency

Postmortem findings :

No lesions in peracute cases

Large amount of clear, straw coloured pericardial fluid

Petechial haemorrhages of the heart muscle

Congestion of the abomasal and intestinal mucosa (Fig. 163)
and liver

Soft pulpy kidneys a few hours after death is characteristic
of this disease

Overload of the rumen and abomasum with concentrate

Haemorrhage and edema in sheep brain

Rapid decomposition of the carcass

Judgement : Carcass of an animal affected with enterotoxaemia
is condemned.

Darkened and cyanotic subcutaneous tissue due to small
blood vessel engorgement (dark appearance of the skin). The
name “Black disease” was derived from this.

Clear straw coloured fluid in the abdominal and thoracic
cavities and in the pericardial sac

Clostridium novyi is an endemic environmental contaminant and
remains latent in the liver, spleen and bone marrow. Immature
liver flukes, by migrating through the liver, cause liver necrosis.
This initiates Cl. novyi spores to germinate and proliferate.
Necrotizing and haemolytic toxins are produced which cause
generalized toxaemia and haemolysis of the blood.

This is a chronic disease of sheep and goats manifested by
abscesses in the lymph nodes. It is caused by Corynebacterium
pseudotuberculosis. Caseous lymphadenitis has a worldwide
distribution and causes great economic losses to the sheep
industry.

Transmission : Discharge from the lymph nodes, via wounds
caused by shearing, castration and docking, contaminated sheep
dips, skin abrasions or traumatized oral mucosa. Animals with
open abscesses should be segregated in order to prevent the
spread of the disease.

Antemortem findings :

Animal is lagging behind the flock.

Dyspnea

Purulent ocular and nasal discharge

Enlarged superficial body lymph nodes

Generalized disease is associated with weight loss,
depression and loss of appetite.

Firm and dry abscess in the kidney (Fig. 166) and other
organs Soft pasty abscess in the early stages changes to firm
and dry with a characteristic laminated appearance in the
later stages of disease.

Abscess content is creamy and pasty in goats

Pneumonia

Differential diagnosis : Abscesses in the organs and viscera,
neoplasm, echinococcosis and other parasitic lesions

Judgement : If this condition is associated with extensive
involvement of many lymph nodes and tissues, suggesting a
haematogenous spread, the carcass is condemned. Otherwise it is
approved. The affected tissue is condemned.

Remarks : An abscess in a body lymph node is a sequel to the
organism gaining entrance into the body via skin wounds etc. The
drained area of the lymph node should be examined. If no other
lesions are observed, it may be an indication that the lymph node
has sequestered the agent. It is not necessary to condemn a quarter
or a carcass due to a lesion in one lymph node or in several lymph
nodes.

Coenurosis is a disease of the brain and spinal cord caused by
the intermediate stage of Taenia multiceps which inhabits the
intestine of dogs, cats and wild carnivores. The clinical disease
occurs in sheep and rarely in cattle.

Life cycle : Eggs expelled with dog faeces are ingested by the
intermediate host (sheep). The larvae hatch in the intestine and
pass with the blood stream towards different organs. The larvae
which reach the brain and spinal cord grow to the coenurid stage.
Coenurus cerebralis will further mature in the brain and spinal
cord.

Hydatid disease occurs in sheep, cattle, swine, horses and
humans. Echinococcosis is a disease which occurs when the larval
stage of Echinococcus granulosus and Echinococcus multilocularis
are ingested by an intermediate host (sheep, cattle). These larvae
then develop into hydatid cysts in various tissues. The adult tape
worms are found in dogs, cats and other carnivores. They may
ingest the hydatid cysts by eating infected organs of the
intermediate hosts. The scolex attaches to the intestinal wall. Adult
tapeworms develop in approximately seven weeks and eggs are
shed in the faeces and are ingested by sheep and cattle. The ova
hatch to liberate the onchospheres which penetrate the intestinal
wall and through the portal venous supply to the liver where they
become arrested. In older sheep and cattle the larvae may reach
the lungs and various other organs through the systemic
circulation. The most common sites of cysts are the liver and
lungs. The cysts are different sizes and shapes and they contain
a clear fluid. Due to the growth of the cyst, pressure atrophy is
noted in the surrounding tissue.

Daughter cysts are found outside the mother cyst and are formed
due to trauma or external pressure on the mother cyst. They may
or may not be attached to the mother cyst. Daughter-cyst
formation may have neoplastic characteristics when there is
penetration to the blood and lymph vessels and metastases to
various distant organs.

Humans gets infected with hydatid disease via the ingestion of
ova from Echinococcus tapeworm in the dog. This usually occurs
by touching dog hair that has been contaminated by ova from
faeces. It also may occur by the dog transferring ova from the
anus to its mouth and then by licking humans.

Judgement : The animal carcass affected with echinococcosis is
approved if edema and emaciation are not found. Otherwise the
carcass is condemned. The affected organs are also condemned and
must be destroyed. The lungs are most commonly affected and
these should be carefully checked because lesions are often missed
on routine inspection.

Dictyocaulus filaria is the common sheep lung worm which
cause verminous pneumonia or bronchitis.

Life cycle : (Fig. 169) Adult worms live in the bronchi where they
lay eggs which are coughed up to pharynx and swallowed by the
host. The eggs are hatched in the digestive tract and the larvae are
then expelled in the faeces. In a moist environment and moderate
temperature, the larve will become infective in 3 – 7 days. Larvae
are rsistant to cold, althourhg it will cause their maturation to be
delayed. Upon digestion by sheep (primary host), larvae penetrate
the intestinal wall and reach the meenteric lymph nodes. From the
mesenteric lymph nodes via the blood stream, larvae migrate to
the lung alveoli and further to the bronchi. They mature in the
bronchi and lay eggs. The cycle is then repeated.

Muellerius capillaris parasitises in the alveoli and pulmonary
parenchyma. Intermediate hosts are snails and slugs which sheep
inget during grazing. Larvae reach the lungs and produce small
greyish nodules on the back of the lungs.

Judgement : Carcass is approved in lung worm infestation if no
secondary changes are observed. The lungs are condemned. If lung
worm infestation has caused pneumonia, emaciation or anaemia,
the carcass is condemned.

The fluke Fasciola hepatica is most frequently found in sheep
and cattle and less often in goats and swine. Acute fascioliasis
occurs almost entirely in sheep. In sheep and cattle, wandering
flukes damage liver tissue and bile ducts which then become
thickened and fibrous.

Life cycle: Thadult flukes of Fasciola hepatica are found in the
bile ducts and gall baladder. The eggs are shed into the bile duct
from which they pass to the intestine. With animal faeces, the eggs
are expelled out on the pasture.

The larve (miracidia) enter aquatic snails (Limnea truncatula)
which are the intermediate hosts and develop into sporocysts and
later into rediae. The rediae will further develop into the final
larval stage (cercaria). Cercaria will transform in the external
environment to metacercaria. If ingested by herbivorous animals,
metacercaria will penetrate the small intestinal wall, cross the
peritoneal space and reach the liver. In the bile ducts, metacercaria
will mature into an adult fluke. The metacercariae which do not
reach the bile ducts will encapsulate in the liver parenchyma.

Fasciloides magna is a large liver fluke which is prevalent in elk,
deer and moose. Sheep and goats are susceptible to infection if
they share the pasture with those wild animals. F. magna in sheep
continuously migrate through the liver parenchyma and may cause
death in less than six months.

Lancet flukes (Dicrocoelium dendriticum) in sheep cause little
damage to the liver parenchyma except for a moderate to marked
thickening of the bile ducts.

Cysticercus tenuicollis is the cystic stage of tape worm Taenia
hydatigena which is found in dogs and cats. Ova pass with dog
faeces on the pasture and may get ingested by intermediate hosts
sheep and pigs. Larvae which develop from ova penetrate the
intestine and pass by portal vein to various tissues especially the
omentum, mesentery, peritoneum and liver. Migration through the
liver leaves greyish-white tortuous tracts. If larvae reach the liver
surface they develop into thin-walled fluid filled bladders and if
they fail they degenerate and become calcified.

Heavy infestation with Cysticercus tenuicollis in young animals
causing liver damage and haemorrhages or peritonitis, rarely
results in the death of the animal.

Antemortem findings :

Moderate to heavy infections produce:-

Loss of appetite

Depression

Weakness

Postmortem findings :

Cysts of different diameters on the liver, diaphragm and
peritoneum

Subserosal cysts on the liver (Fig. 172)

Judgement : The carcass affected with cysticercus tenuicollis is
approved. The organs are condemned and affected serous
membranes should be stripped.

Cysticercus ovis is the larval stage of Taenia ovis, a tapeworm
found in the intestines of dogs and wild carnivores. Its
development is similar to that of Taenia saginata. However, in the
case of Taenia ovis, the definitive hosts are sheep. The cysts are
found in the heart, diaphragm, masseters and the skeletal
musculature of sheep. They are fully developed from 7 to 10
weeks after the ingestion of the ova. The rapid degeneration of
cysts commence almost immediately after the cysts reach
maximum development. When degenerated, the cysts appears as
a caseous nodule in the musculature.

Antemortem findings : Usually no clinical signs are recognized.

Postmortem findings :

The cysts are oval, measure 9 mm × 5 mm when fully
developed and are most common in the heart (Fig. 173), the
masseters, the diaphragm and the skeletal musculature (Fig.
174).

In older animals the cysts degenerate and calcify

The degenerated cysts appears as greenish yellow caseous
nodules with calcification often present.

Judgement : In moderate or light infestation consisting of a small
number of dead or degenerated cysticerci, the carcass can be
boned out under supervision, the cysts removed and the meat
passed after being held for 10 days at -10°C. If the freezing
treatment is not possible, the heating of the carcass at 56°C is
suggested.

In heavy infestations the carcass is condemned. It is commonly
considered that an animal is heavily infested if lesions are
discovered in two of the usual inspection sites including the
masseter muscle, tongue, oesophagus, heart, diaphragm or exposed
musculature and in two sites during incision into the shoulder and
the rounds. Carcasses with C. ovis infestations may not be
acceptable for export.

This is a tape worm which occurs in the bile duct of sheep, goats
and wild ruminants. The life cycle is not completely known but
oribatid mites are suspected of transmitting the parasites. The
parasite affects animals of all ages and is considered non
pathogenic. Heavy infections are frequently seen in apparently
healthy sheep. With almost complete occlusion of the bile ducts,
icterus and the other clinical signs are not observed. There are
areas where approximately 80 % of sheep and goat livers are
affected.

Judgement : The carcass is approved unless associated with
emaciation. The affected liver is condemned. In some parts of the
world, all sheep livers are condemned on postmortem inspection,
because of high rate of liver infections.

Fig. 175:
Stilesia
hepatica. Long,
threadlike
parasite (20-50
cm long and up
to 3 mm wide)
in the sheep
liver.

In sheep and goats, babesiosis is caused by Babesia motasi and
Babesia ovis. Acute signs of the disease are characterized with
fever, anaemia, parasitemia and haemoglobinuria. B. ovis usually
causes a milder form of the disease than does B. motasi. The
parasite grows and multiplies in the blood corpuscles
(erythrocytes) of sheep and goats and causes haemoglobin
(constituent of erythrocytes) elimination in urine
(haemoglobinuria).

Transmission : Different species of ticks in the family Ixodidae
serve as vectors of infection. Babesia ovis infection transmitted
experimentally in sheep has caused acute signs of disease,
parasitemia and lasting immunity similar with babesiosis in cattle.

Antemortem findings :

Incubation 7 – 10 days

High fever (41.5°C)

Difficult breathing

Anaemia

Loss of appetite

Dark reddish brown urine

Recovered animals may be emaciated, have reduced milk
production, and some may also abort.

Subcutaneous tissue and connective tissue in the muscles are
edematous and jaundiced.

Thin watery blood and red urine in the bladder

Enlarged spleen

Edematous and haemorrhagic lymph nodes

Judgement : Carcass of an animal in the subclinical form of the
disease or in the chronic stage may have a favourable judgement
providing the carcass is adequately set and icterus is not present.
An animal carcass showing acute form of the disease accompanied
with fever, marked anaemia and haemoglobinuria and/or
emaciation is condemned.

Toxoplasmosis is a contagious disease of animals and man
caused by protozoon Toxoplasma gondii. It is found most
frequently in pigs and sheep. Toxoplasma in sheep is manifested
with abortion and stillbirths in ewes.

Life cycle : see Fig. 147

Antemortem findings:

Abortion and stillbirths in ewes

Fever

Generalized tremor

Difficult breathing

The systemic disease is seldom found in sheep.

Postmortem findings:

Multiple granulomatous lesion in the lungs

Hydrothorax

Ascites

Intestinal ulceration

Necrosis in the liver, spleen and kidneys

Necrosis of placenta

Brain haemorrhage, edema and ventricular dilatation (Fig.
176)

Inflammation of the brain (Fig. 177)

Judgement: Carcass of an animal showing clinical signs of acute
disease is condemned. Recovered and reactor animals are
approved.

Theileriosis is thick borne disease of sheep and goats, cattle,
buffalo and wild ruminants caused by species of protozoa in the
genus Theileria. In sheep and goats, the infections are caused by
T. hirci and T. ovis. Theileria hirci is the cause of an acute and
highly fatal disease of sheep and goats in Eastern Europe, the
Middle East, Asia and North Africa. The subacute and chronic
forms have also been reported. Mild infection in noted young
lambs and kids. Theileria ovis causes a milk disease in sheep and
goats; a disease from which they rapidly recover.

Transmission : The thick vector is unknown in Theileria hirci
infection, although Hyalomma spp. are suspected.

Antemortem findings :

In acute form

Morbidity rate of 100 % and mortality of 46 – 100 %

Fever (40°C - 41°C)

Loss of appetite and listlessness

Increased heart rate and difficult breathing

Edema of the throat and subsequent death

Hyperaemia of the conjunctiva and nasal discharge

Swollen superficial lymph nodes

Atony of the rumen in the chronic form

Mild fever, anaemia, icterus, weakness and emaciation

Postmortem findings :

The lesions are basically similar as those observed in bovine
Theileriosis (T. parva).

Edema of the lungs

The yellowish-brown liver may be increased in size and
shows soft and friable consistency.

Judgement : Carcass and viscera of an animal showing clinical
signs of chronic theileriosis and being without gross lesions, are
approved. If the acute form of the disease is accompanied with
fever, icterus and generalized lesions, the carcass and organs are
condemned.

Sarcocystosis of sheep is a widespread infestation caused by four
species of Sarcocystis (Table 2). Nearly all adult sheep in most
parts of the world are infested. Three other species of Sarcocystis
have been described from goats. Their prevalence and importance
in meat inspection are not fully known.

The general pattern of the life-cycle is similar to that described
for Sarcocystis cruzi in cattle except that each species uses its own
definitive hosts. S. tenella and S. gigantea cause the most
widespread infestations. S tenella produces microcysts and are the
most pathogenic. S. gigantea produces macrocysts and are
generally not pathogenic but because of their large size they are
important in meat inspection.

Table 2: Sarcocystis spp. in sheep

Species

Distribution

Definitive Hosts

Size and Shape of Cyst

Pathogenicity

Sarcocystis tenella

World-wide

Dog, coyote and red fox

Microscopic, up to 0.7 mm long, may be found in the central nervous system

Pathogenic. Causes anorexia, weight loss, anaemia, fever, abortion and even death. It is the most pathogenic sheep Sarcocystis sp.

Sarcocystis gigantea

World-wide

The domestic cat

Macroscopic, oval or elongated and measures up to 1 cm long, More common in order sheep.

Only mildly pathogenic.

Sarcocystis arieticanis

Europe, Australia, New Zealand and the USA

Dog

Microscopic, up to 0.9mm long.

They are less pathogenic than S. tenella

Sarcocystis medusiformis

Australia and New Zealand

Cat

Macroscopic, filiform and elongated up to 8mm long and 0.2mm wide.

Pathogenicity not known.

Antemortem findings (in S. tenella infection):

Fever

Anaemia

Loss of appetite and weight loss

Retarded growth

Enlarged lymph nodes

Abortion

Nervous signs

Postmortem findings (in S. gigantea infestations) :

Oval, elongated or fusiform cysts up to 1 cm long and 0.5
cm wide in the oesophagus (Fig. 178), pharynx, diaphragm,
skeletal musculature, tongue and heart

In S. tenella infestations haemorrhages in the serous surface
of the viscera, cardiac and skeletal muscles

Serous atrophy of pericardial and perirenal fat

Judgement : In heavy infestations the carcass is condemned. In
moderate to light infestations the lesions are removed and the
carcass is passed.